Antipsychotics & Mood Stabilizers Flashcards
Schizophrenia: affects how many ppl, sxs appear when
affects abt 1 in 100 ppl
sxs appear during late adolescents or early adulthood
“Positive” sxs of schizophrenia: controlled by, due to, & what are they
controlled fairly well by classical antipsychotic drugs
- due to ↑DOPAMINERGIC ACTIVITY IN THE LIMBIC SYSTEM
- abnormality or exaggeration of normal fxn (incoherent speech, agitation)
- hallucinations (U) auditory, delusions, bizarre behaviot & thought d/os
“Negative” sxs of SCZ: controlled by, due to & what are the sxs
sxs respond to new gen. “atypical” antipsychotics
- due to DECREASED DOPAMINERGIC ACTIVITY IN FRONTAL CORTEX
- loss or decrease in fxn (little or no speech, blunted emotions), lack of affect, lack of volition, apathy, lack of pleasure, ASOCIAL not antisocial behavior like the handout says
Cognitive impairment in SCZ: controlled by & sxs
these sxs do not respond well to current therapies
sxs: inability to pay attention, distraction may impair memory of recent events, disorganized speech, thought, neologisms, memory loss
Dopaminergic hypothesis of SCZ
- DA D2 receptor blocking activity correlates with antipsychotic potency
- PET scanning has shown in ↑ in DA receptors in tx & untx schizoprenics
- SEROTONIN may also be involved as drugs that stimulate 5HT2A receptors (LSD) can cause hallucinations and those that block these receptors (antagonists) are effective txs)
Mesolimbic pathway
projects from VTA to LIMBIC SYSTEM
a/w higher mental fxn & emotions
OVER-STIMULATION results in POSITIVE sxs of SCZ
Mesocortical pathway
projects from VTA to FRONTAL CORTEX
higher mental fxn & emotions
UNDER-STIMULATION results in NEGATIVE sxs of SCZ
Nigrostriatal pathway
projects from substantial nigra to caudate/putamen
primary role: control of posture & voluntary movement
↓ in activity produces sxs of Parkinson’s dz & EXTRAPYRAMIDAL SYMPTOMS (PD-symptoms induced by drugs)
Tuberoinfundibular pathway
projects from hypothalamus to anterior pituitary
reg. prolactin release, DA inhibits secretion of prolactin
Classical Antipsychotics: mechanism of action
block DA D2 receptor
inhibits DA release in mesolimbic pathway=relieves positive sxs of SCZ
potency for blocking DA D2 correlates with efficacy of relieveing POSITIVE sxs of SCZ
but NO EFFECT ON NEG SXS
Atypical Antipsychotics: mechanisms of action
block 5HT2A receptors in addition to DA receptors
5-HT receptor blockers ↑ DA release in MESOCORTICAL PATHWAY
so tx both neg & pos
most also block muscarinic, alpha-adrenergic & histamine receptors in the brain & periphery=the basis of many SEs
Pharmacological Effects of antipsychotics (as a broad class)
↓ fear, hostility, agitation, hallucinations, delusions
slows psychomotor fxn, may ↓ restlessness & anxiety
↓initiative & interest in environment, as do emotions
↓aggressiveness & disrupted behaviors
ANTIEMETIC activity occurs from blockage of DA receptors in CTZ
Antipsychotic SEs
fairly safe, high therapeutic index, unpleasant SEs
sleepiness, restlessness, weight gain, autonomic sxs
EPS, TD, endocrine abnormalities
Extrapyramidal Symptoms (EPS): what causes them, what are they
D2 antagonists also block DA receptors in nigrostriatal system (substantia nigra, striatum); these areas imp for motor control->EPS
AKATHISIA: anxiety, restlessness, pacing, constant rocking
DYSTONIA: involuntary muscle spasms, sustained abnormal postures of limbs, trunk, face, tongue
PARKINSONIAN SXS: tremor, rigidity, difficulty initiating movement
Which drugs antipsychotics have less tendency to cause EPS? Why?
atypicals, like clozapine and risperdone b/c they have ↓ affinity for D2 receptors; bind instead to 5-HT2A &/or D4 receptors